Vomiting and Malabsorption in Children Flashcards
Types of vomiting
Vomiting with retching
Projectile vomiting
Bilious vomiting
Effortless vomiting
Phases and features of these phases of vomiting with retching
Pre-ejection phase
- pallor
- nausea
- tachycardia
Ejection phase
- retch
- vomit
Post-ejection phase
- weakness, pale and limp
- shivering
- lethargy
What stimulates vomiting centre?
enteric pathogens Intestinal inflammation Metabolic derangement Infection Head injury Visual stimuli Middle ear stimuli
Features of bilious vomiting
Should always ring alarm bells
Due to intestinal obstruction until proven otherwise
Causes of bilious vomiting
Intestinal atresia Malrotation +/- volvulus Intussusception Ileus Crohn's disease with strictures
Investigations of bilious vomiting
Abdominal x-ray
Consider contrast meal
Surgical opinion re exploratory laparotomy
Daily, how much fluid enters the duodenum, and how much of this gets to the colon and is lost in faeces?
9L enters duodenum each day
1.5L gets to colon
< 200ml lost in faeces
What causes the 600-fold increase in surface area of the small intestine?
Mucosal folds
Villi
Essential secretory component of GI tract
Water for fluidity/enzyme transport/absorption
Ions
Defence mechanism against pathogens
Features of pyloric stenosis
Babies 4-12 weeks old Boys > girls Projectile non-bilious vomiting Weight loss Dehydration +/- shock
Characteristic electrolyte disturbance in pyloric stenosis
Metabolic acidosis
Hypocholoraemia
Hypokalaemia
Features of gastro-oesophageal reflux
Movement of gastric contents into the oesophagus - GORD occurs when this causes inflammation
Effortless vomiting
Very common problem in infants
Usually self-limiting and resolves spontaneously
Presenting symptoms of gastro-oesophageal reflux/GORD
Gi
- vomiting
- haematemesis
Nutritional
- feeding problems
- failure to thrive
Respiratory
- apnoea
- cough
- wheeze
- chest infections
Neurological
- Sandifer’s syndrome
What is Sandifer’s syndrome?
Association of GORD with spastic torticollis and dystonic body movements
Nodding and rotation of the head, neck extension, gurgling sounds, writhing movements of limbs and severe hypotonia have been reported
Causal relation between GORD and neurological manifestations of Sandifer’s syndrome is supported by the resolution of the manifestations on successful treatment of GORD
Medical assessment of GORD
History and examination often sufficient
Radiological investigations
- Video fluoroscopy (only if swallowing problems)
- Barium swallow
pH study - gold standard
Oesophageal impedance monitoring
Endoscopy if not resolved in 2 years or severe symptoms
What features or GORD can be picked up on radiology?
Dysmotility
Reflux
Gastric emptying
Strictures
Treatment of gastro-oesophageal reflux
Feeding advice
Nutritional support
Medical treatment
Surgery
Feeding advice for gastro-oesophageal reflux
Feed thickeners e.g. carobel
Appropriateness of foods - texture and amount
Behavioural programme - oral stimulation, removal of aversive stimuli
Feeding position - 45 degrees
Nutritional support for gastro-oesophageal reflux
Calorie supplements
Exclusion diet
Nasogastric tube
Gastrotomy
Medical treatment of gastro-oesophageal reflux
Feed thickener e.g. gaviscon
Prokinetic drugs
Acid-suppressing drugs
Indications for surgery for gastro-oesophageal reflux
Failure of medical treatment
Persistent
- failure to thrive
- aspiration
- oesophagitis
Vomiting without complications is not an indication
Features of Nissen Fundoplication
Children with cerebral palsy are more likely to have complications of bloat, dumping and retching after surgery
Successful surgery may unmask more generalised GI motility problems in the child
Post-operative course may be more complicated in children with cerebral palsy
Chronic diarrhoea definition
4 or more stools per week
- < 1 week = acute diarrhoea
- 2-4 weeks = persistent diarrhoea
- > 4 weeks = chronic diarrhoea
Causes of chronic diarrhoea
Motility disturbance
- toddler’s diarrhoea
- irritable bowel syndrome
Active secretion
- acute infective diarrhoea
- IBD
- secretory
Malabsorption of nutrients
- food allergy
- CF
- coeliac disease
- osmotic
Features of osmotic diarrhoea
Movement of water into the bowel to equilibrate osmotic gradient
Usually a feature of malabsorption - enzymatic defect or transport defect
Mechanism of action of lactulose/movicol
Generally accompanied by macroscopic and microscopic intestinal injury
Clinical remission with removal of causative agent
Types of carbohydrate malabsorption
Primary lactose malabsorption very rare Secondary lactose malabsorption e.g. rotavirus infection Glucose-galactose malabsorption Fructose malabsorption Disaccharidases deficiency
Causes of fat malabsorption
Pancreatic Disease
- Diarrhoea due to lack of lipase and resultant steatorrhoea
- Classically cystic fibrosis
Hepatobiliary Disease
- Chronic liver disease
- Cholestasis
Features of secretory diarrhoea
Classically associated with toxin production from vibrio cholerae and enterotoxigenic E. coli - in cholera, can lose 24L per day
Intestinal fluid secretion predominantly driven by active Cl- secretion via CFTR
Features of motility diarrhoea
Classically toddler’s diarrhoea
Other causes - irritable bowel syndrome, congenital hyperthyroidism, chronic intestinal pseudo-obstruction
Features of inflammatory diarrhoea
Mixed bag
Malabsorption due to intestinal damage
Secretory effect of cytokines
Accelerated transit time in response to inflammation
Protein exudate across inflamed epithelium
Important features of history of a child with diarrhoea
Age at onset Abrupt/gradual onset Family history Nocturnal defaecation - suggests organic pathology Consider growth and weight gain of child
Components of faeces analysis
Appearance
Stool culture
Determination of secretory vs osmotic
What percentage of Western population are affected by coeliac disease?
1%
Presentation of coeliac disease
Abdominal bloating Diarrhoea Failure to thrive Short stature Constipation Tiredness Dermatitis herpatiformis
Susceptible asymptomatic group to coeliac disease
Type 1 DM
Autoimmune thyroid disease
Down syndrome
First degree relatives of people with coeliac disease
Screening tests for coeliac disease
Serological screens
- anti-tissue transglutaminase
- anti-endomysial
- concurrent IgA deficiency in 2% may result in false negatives
Gold standard - duodenal biopsy
Genetic testing - HLA DQ2, DQ8
ESPCHAN/BSPCHAN Guidelines for coeliac disease
Symptomatic children Anti-TTG > 10 times upper limit of normal Positive anti-endomysial antibodies Normal serum IgA HLA DQ2, DQ8 positive Diagnose coeliac disease without biopsy
Treatment of coeliac disease
Strict gluten-free diet for life - avoid rye, wheat and barley
Gluten must not be removed prior to diagnosis as serological and histological features will resolve
In very young (< 2 years) re-challenge and re-biopsy may be warranted
Increased risk of rare small bowel lymphoma if untreated
